Discussion
We have learned significant lessons from this unique complication.
Iatrogenic VSD in the setting of systemic RVAD causes significant
hypoxia due to the significant inflow suction by the VAD from the
pulmonic ventricle, resulting in a right-to-left shunt. The iatrogenic
VSD was effectively treated with VSD patch closure, a similar technique
that is employed for a post-infarction VSD. The second significant
challenge was persistent right-to-left shunt and desaturation despite
having adequate VSD patch and a small patch leak, highlighting the
clinical significance of even small shunts after VAD implantation. This
is likely due to the combination of high negative pressure from the
inflow cannula in the morphologic RV and dysfunctional and distended
subpulmonary left ventricle. The mechanism of the remarkable effect of
iNO in our case is somewhat unclear, but perhaps explained by reduction
of the afterload and subsequent improved ventricular ejection and
decompression of the subpulmonary LV.
Determining the favourable positioning of the inflow cannula in ccTGA is
a technical challenge. Using routine TEE offers guidance for cannula
insertion in most VAD cases, but was not sufficient in preventing
iatrogenic injury in this case. The authors would recommend more
detailed pre-planning using cross-sectional imaging, such as computed
tomography or magnetic resonance imaging, and the addition of epicardial
studies for seating the VAD inflow. Although extremely rare, iatrogenic
VSDs have been well reported in adults.2,3 Barioliet al describes acute VSD creation during septal myectomy for
hypertrophic obstructive cardiomyopathy that was initially repaired
intraoperatively with a large bovine pericardial patch, with delayed
percutaneous closure of residual VSD using the Amplatzter
multi-fenestrated septal occluder.4 Successful
transcatheter iatrogenic VSD closure after aortic valve replacement has
also been well described.5 In our case, the acute
desaturation from a large iatrogenic VSD was managed intraoperatively
with patch repair, RVAD revision, and the addition of supplementary iNO.
The possibility of percutaneous intervention for the residual shunt was
discussed. However, considering the technical difficulty of device
closure near a VAD inflow and the relative improvement of the patient’s
clinical status with iNO, further procedural intervention was deferred.
The presence of the VSD patch and residual shunt did necessitate an
earlier listing for heart transplantation postoperatively compared to
patients with uncomplicated VAD placement. This case highlights a unique
iatrogenic complication during VAD implantation in a patient with
complex congenital heart disease, and the management steps that were
taken to troubleshoot hemodynamic instability.